The effects of hyperthermia on human baroreflex control of blood pressure are unknown. Hyperthermia increases sympathetic activity in humans evidenced by increases in cardiac output, heart rate, splanchnic and renal vascular resistances, and muscle sympathetic nerve activity. Since baroreceptor control of these variables is described by a sigmoidal relationship between changes in these efferent variables relative to changes in blood pressure, the PI suggests that the functional reserve to further increase these variables during a hypotensive challenge will be reduced in hyperthermia if the respective baroreflex curves are not adjusted. Thus, the following, hypothesis will be tested: hyperthermia alters baroreceptor control of blood pressure in humans. Studies have shown that hyperthermia attenuates alpha- adrenoceptor responsiveness in both intact animals and isolated vessels. Similar studies have not been conducted in humans. If alpha-adrenoceptor responsiveness in humans is likewise attenuated in this environment, baroreceptor adjustments to a reduction in blood pressure in hyperthermia will be less effective in maintaining pressure since end organ vascular responses are attenuated. Therefore, studies will be conducted to test the hypothesis that hyperthermia decreases alpha- adrenoceptor responsiveness in humans. A primary function of baroreflexes is to maintain blood pressure to adequately perfuse the cerebral circulation. The cerebral circulation has a wide autoregulatory range in which large changes in perfusion pressure do not appreciably change cerebral blood flow. Sympathetic stimulation shifts both the lower and upper limits of this autoregulatory curve to higher pressures. Such a shift reduces the reserve to maintain cerebral blood flow during reductions in perfusion pressure, and may predispose the individual to syncope during a hypotensive challenge. As previously mentioned, hyperthermia increases sympathetic activity, and therefore may decrease the reserve to maintain cerebral blood flow during reductions in perfusion pressure in this environment. Thus, the following hypothesis will be tested: hyperthermia shifts the cerebrovascular autoregulatory curve to higher pressures resulting in impaired autoregulation of cerebral blood flow to decreases in perfusion pressure. To address these issues, integrated and individual baroreflex function will be assessed in normothermia and hyperthermia, as will alpha-adrenoceptor responsiveness in both skin and muscle. Finally steady state and dynamic cerebrovascular autoregulation will be assessed in normothermia and hyperthermia using transcranial Doppler.